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August 1972

Acute Pancreatitis and Hyperamylasemia in Renal Homograft Recipients

Author Affiliations

From the Department of Surgery, University of Colorado School of Medicine, and the Veterans Administration Hospital, Denver. Dr. Durst is now with Hadassah Hospital, Jerusalem, Israel. Dr. Machado is now with Universidade de Sao Paulo, Brazil.

Arch Surg. 1972;105(2):167-172. doi:10.1001/archsurg.1972.04180080021004

In a series of 301 renal homograft recipients, 17 (5.6%) had acute pancreatitis at some time after transplantation. Eleven of these patients died, for a mortality of 64.7%. In each instance, pancreatitis was a major factor in a complex chain of lethal events to which immunosuppression invariably contributed. An additional 43 patients (14.3%) developed asymptomatic hyperamylasemia after transplantation and, undoubtedly, some of these recipients also had pancreatitis. The factors causing pancreatitis in the renal transplantation patient include uremia, hyperparathyroidism, pancreatic injury by drugs, infections resulting from chronic immunosuppression, gallstones, and operative trauma to the pancreas. In cases of preexisting pancreatitis, transplantation is not necessarily precluded, but efforts should be made to find a specific cause of the pancreatitis and take corrective measures, such as biliary tract surgery or parathyroidectomy if indicated, in advance of transplantation.

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